Lyme disease, named after the site of an epidemic of oligoarticular arthritis [Steere et al., Arthritis Rheum. 20: 7-17 (1977)], is a multisystem infection often accompanied by an expanding skin lesion (erythema migrans) and concomitant or subsequent development or arthritic, cardiac, or neurologic complications [Reik et al., Medicine 58:281-294 (1979); Steere et al., Ann. Intern. Med 93 (1): 8-16 (1980); Steere et al., Ann. Intern. Med. 86:685-698 (1977); Steere et al., Ann. Intern. Med. 107: 725-731 (1987)]. Subsequent epidemiological studies have identified the deer tick, Ixodes dammini, as the primary vector of Lyme disease in North America [Burgdorfer et al., Science 216 1317-1319 (1982)] and a spirochete, Borrelia burgdorferi (hereinafter "B. burgdorferi"), as the causative agent of Lyme disease [Anderson et al., Am. J. Trop. Med. 32:818-824 (1983); Steere et al., N. Engl. J. Med. 308:733-740 (1983)]. Lyme disease is now the most common tick-borne illness recognized in the United States [Habicht et. al., Sci. Am. 257:78-83 (1987)].
Since Lyme disease may be more successfully treated if diagnosed early, an effective clinical assay for the detection of exposure to or infection with B. burgdorferi has been sought. Several prior assays, which rely on determination of the titer of antibodies to B. burgdorferi in patient sera, have used fluorescent-labelled anti-IgG antibodies [e.g., Magnarelli et. al., J. Clin. Microbiol. 20:181-184 (1984); Russell et al., J. Infect. Dis. 149:465-470 (1984); Steere et al., N. Engl. J. Med. 308: 733-740 (1983); Stiernstedt et al., J. Clin. Microbiol. 21: 819-825 (1985); Pennell et al., J. Clin. Microbiol. 25: 2218-2220 (1987)] and enzyme-labelled anti-IgG antibodies [e.g., Craft et al., J. Infect. Dis. 149: 789-795 (1984); Magnarelli et al., J. Clin. Microbiol. 20:181-184 (1984); Russell et al., J. Infect. Dis. 149: 465-470 (1984); Stiernstedt et al., J. Clin. Microbiol. 21: 819-825 (1985); Berardi et al., J. Infect. Dis. 158: 754-760 (1988)] to detect anti-B. burgdorferi antibodies which had previously been immobilized on a solid phase by binding to B. burgdorferi antigen. Unfortunately, these assays are of limited clinical use, since these antibody titers may not accurately indicate when the patient was exposed to B. burgdorferi. Furthermore, in many cases antibodies are not detected in patient sera by such assays until major symptoms of Lyme disease begin to appear making effective treatment more difficult if not impossible. In addition, these assays fail to define the immune status of the host or to predict the response of the host to infection or re-infection. It would, therefore, be desirable to provide an assay for exposure to or infection with B. burgdorferi which is capable of more accurate and more contemporaneous (i.e., closer to the date of exposure or infection) detection and which is capable of defining the immune status of a patient.